Experimental autoimmune uveoretinitis (EAU) was induced in Cynomolgus monkey by immunization with recombinant human retinal S-antigen. At the onset of ocular disease, animals were treated for 28 days with intravenous injection of humanized anti-Tac, an anti-interleukin (IL)-2 receptor antibo originally produced in mouse but modified by replacing all but its binding region with human immunoglobulin elements. Controls were treated with vehicle alone. The animals were examined twice a week during the treatment period. The progression of the disease was markedly limited in the group treated with anti-Tac-H, while the severity of the inflammation continued t increase in the control group. The in vivo results were correlated with a significant inhibition of monkey lymphocyte proliferation stimulated by IL- when anti-Tac-H was added to the culture medium.